Types of Wound Healing

Wounds are
classified by the way the wound closes. A wound can close by primary
intention, secondary intention or tertiary intention.

1. Primary
Intention

Primary
healing involves reepithelialization, in which the skin's outer layer grows
closed. Cells grow in from the margins of the wound and out from epithelial
cells lining the hair follicles and sweat glands.
(Johnstone, Farley,& Hendry, 2005)

Wounds that
heal through primary intention are, most commonly, superficial wounds that
involve only the epidermis and don't involve the loss of tissue, for example,
a first-degree burn. However, a wound that has well-approximated edges (edges
that can be pulled together to meet neatly), such as surgical incision, also
heals through primary intention. Because there is no loss of tissue and little
risk of infection, the healing process is predictable. These wounds usually
heal in 4 to 14 days and result in minimal scarring.
(Slachta, 2003)

A wound that
involves some degree of tissue loss heals by secondary intention. The edges of
these wounds can't be easily approximated, and the wound itself is described
as partial thickness or full thickness, depending on its depth:
(Johnstone, Farley,& Hendry, 2005)

Partial-thickness wounds extends through the epidermis and into, but not
through, the dermis.

During
healing, wounds that heal by secondary intention fill with granulation tissue,
a scar forms, and reepithelialization occurs, primarily from the wound edges.
Pressure ulcers, burns, dehisced surgical wounds, and traumatic injuries are
examples of this type of wound. These wounds also take longer to heal, result
in scarring, and have a higher rate of complications than wounds that heal by
primary intention. (Slachta, 2003)

When a wound
is intentionally kept open to allow edema or infection to resolve or to permit
removal of exudate, the wound heals by tertiary intention, or delayed primary
intention. These wounds result in more scarring than wounds that heal by
primary intention but less than wounds that heal by secondary intention.
(Johnstone, Farley,& Hendry, 2005)

Normal wound
healing occurs in four phases: the hemostasis, the inflammation, the
proliferation and the maturation. However, healing rarely occurs in this
strict order. Typically, the phases of wound healing overlap.
(Slachta, 2003)

1. Hemostasis

Immediately
after an injury, the body releases chemical mediators and intercellular
messengers called growth factors that begin the process of cleaning and
healing the wound.
(Harvey, 2005)

When blood
vessels are damaged, the small muscles in the walls of the vessels contract,
reducing the flow of blood to the injury and minimizing blood loss.
Vasoconstriction can last as long as 30 minutes.
(Harvey, 2005)

Next, blood
leaking from the inflamed, dilated, or broken vessels begin to coagulate.
Collagen fibers in the wall of the damaged blood vessels activate the
platelets in the blood in the wound. Aided by the action of prostaglandins,
the platelets enlarge and stick together to form a temporary plug in the blood
vessel, which helps prevent further bleeding. The platelets also release
additional vasoconstrictions, such as serotonin, which help to prevent further
blood loss. Thrombin forms in a cascade of events stimulated by the platelets,
and a clot forms to close the small vessels and stop bleeding.
(Johnstone, Farley,& Hendry, 2005)

This initial
phase of wound healing occurs almost immediately after the injury occurs and
works quickly (within minutes) in small wounds. It's less effective in
stopping the bleeding in larger wounds.
(Johnstone, Farley,& Hendry, 2005)

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2.
Inflammation

This phase is
both a defense mechanism and a crucial component of the healing process.
During this phase, the wound is cleaned and the process of rebuilding begins.
This phase is marked by swelling, redness, and heat at the wound site.
(Johnstone, Farley,& Hendry, 2005)

Vascular
permeability increases, permitting serous fluid carrying small amounts of cell
and plasma protein to accumulate in the tissue around the wound (edema). The
accumulation of fluid causes the damaged tissue to appear swollen, red, and
warm to touch.
(Johnstone, Farley,& Hendry, 2005)

During the
early phase of the inflammatory process, neutrophils (one type of white blood
cell) enter the wound. The primary role of neutrophils is phagocytosis, or the
removal and destruction of bacteria and other contaminants.
(Harvey, 2005)

As neutrophil
infiltration slows, monocytes appear. Monocytes are converted into activated
macrophages and continue the job of cleaning the wound. The macrophages play a
key role early in the process of granulation and reepithelialization by
producing growth factors and by attracting the cells needed for the formation
of new blood vessels and collagen.
(Johnstone, Farley,& Hendry, 2005)

The
inflammatory phase of healing is important for prevent wound infection.

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3.
Proliferation

During the
proliferative phase, the body:
(Johnstone,
Farley,& Hendry, 2005)

fills the
wounds with connective tissue (granulation)

contracts
the wound edges (contraction)

covers the
wound with epithelium (epithelialization)

The
proliferative phase involves regeneration of blood vessels (angiogenesis) and
the formation of connective or granulation tissue. The development of
granulation tissue requires an adequate supply of blood and nutrients.
Endothelial cells in blood vessels in surrounding tissue reconstruct damaged
or destroyed vessels by first migrating and then proliferating to form new
capillary beds. As the beds form, this area of the wound takes on a red,
granular appearance.
(Harvey,
2005)

During this
phase, growth factors prompt fibroblasts to migrate to the wound. Fibroblasts
are the most common cell in connective tissue; they are responsible for making
fibers and ground substance, also known as extracellular matrix, which
provides support to cells. At first, fibroblasts populate just the margins of
the wound, they later spread over the entire wound surface.
(Johnstone,
Farley,& Hendry, 2005)

Fibroblasts
have the important task of synthesizing collagen fibers which, in turn,
produce keratinocyte, a growth factor needed for reepithelialization. This
process necessitates a delicate balance of collagen synthesis and lysis
(making new and removing old). If the process yields too much collagen,
increased scarring results. If the process yields too little collagen, scar
tissue is weak and easily ruptured.
(Harvey,
2005)

Complete
healing occurs only after epithelial cells have completely covered the surface
of the wound. As this occurs, keratinocytes switch from a migratory mode to a
differentiative mode. The epidermis thickens and becomes differentiated, and
the wound is closed. Any remaining scab comes off and the new epidermis is
toughened by the production of keratin, which also returns the skin to its
original colour.
(Johnstone,
Farley,& Hendry, 2005)

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4.
Maturation

The final
phase of wound healing takes place when wound remodeling occurs. There is a
diminution of the vasculature and an enlargement of the collagen fibers, which
increase the tensile strength of the repair. This is a gradual, transitional
phase of healing that can contribute for months or even years after the wound
has closed.(Johnstone,
Farley,& Hendry, 2005)

During this
phase, fibroblasts leave the site of the wound, the scar shrinks and becomes
pale, and the mature scar forms. If the wound involved extensive tissue
destruction, the scar won't contain hair, sweat, or subaceous glands. The time
frame for wound maturation, under optimal wound healing conditions is 21 days
to 2 years. The wound gradually gains tensile strength. In primary intention
wounds, tissue will achieve approximately 20% of the original strength between
days 1 and 7. When fully healed, tissue will achieve, at best, approximately
70-90% of its original strength. The longer it takes for a wound to heal, the
more likely it is for scarring to occur. Scar tissue will always be less
elastic than the surrounding skin and is never as strong as the original
intact skin.
(Johnstone,
Farley,& Hendry, 2005)

The wound healing process is affected by many factors. The
most important influences include:
(Slachta, 2003)

Nutrition

Protein is crucial for
repair and synthesis of body tissue.
Carbohydrates: are converted into glucose, the body's preferred source of
energy and is a substrate for wound healing.
Fat is a component of cell membranes and play a role in the inflammatory
process.
Vitamins C, B-complex, A and E.
The minerals iron, copper, zinc, and calcium.
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Oxygenation

Oxygen is crucial for
leukocytes to destroy bacteria and for fibroblasts to stimulate collagen
synthesis.
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Infection

It delays wound healing.
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Aging

Poor nutrition, hydration
and poorer oxygenation, etc.
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Chronic Health Conditions

They can increase the
risk of wounds and interfere with wound healing. They can interfere with
systemic and peripheral oxygenation and nutrition, which affect healing.
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Medications

Such as steroids and
chemotherapeutic agents, reduce the body's ability to mount an appropriate
inflammatory response. This interrupts the inflammatory phase of healing and
can dramatically lengthen healing time.
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Smoking

Carbon monoxide, a
component of cigarette smoke, binds to the hemoglobin in blood in the place
of oxygen. This significantly reduces the amount of oxygen circulating in
the bloodstream, which can impede wound healing. To some extent, this
reaction also occurs in people regularly exposed to second-hand smoke.
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Temperature

Theoretically the optimal
temperature for wound healing is 37oC. If a person's core temperature falls to less than
30oC, tissue damage
occurs. If temperature rise above 40oC, healing halts.
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Stress Level

High stress levels cause
an increased cortisol production, which reduces the number of circulating
lymphocytes, which in turn reduces the inflammatory response.
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Blood Glucose Levels

BGL should be below
200mg/dl for satisfactory healing, regardless of the cause of the wound.
Levels of 200mg/dl or more can impair the function of white blood cells,
which help prevent infection and are important in wound healing.
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DesiccationA moist environment
allows wounds to heal faster and less painfully than a dry environment, in
which cells typically dehydrate and die. This causes a scab or crust to form
over the wound site, which impedes healing. If the wound is kept hydrated
with a moisture-retentive dressing, epidermal cell migration is enhanced,
encouraging epithelialization.
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NecrosisDead, devitalized or
necrotic tissue can delay healing. Slough and eschar are the
two types of necrotic tissue that may appear in a wound. Slough is moist,
loose, stringy necrotic tissue that's typically yellow. Eschar, which
appears as dry, thick, leathery tissue, may be black. In most cases,
necrotic tissue must be removed before repair and healing can occur.

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Wound-Healing
Complications

Unfortunately,
not all wounds heal. The most common complications of healing include:
(Slachta, 2003)

InfectionDrainage of purulent
material and inflamed wound edges that, if uncontrolled, can lead to
osteomyelitis, bacteremia, and sepsis.
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HemorrhageInternal hematoma or
external bleeding.
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DehiscenceSeperation of skin and
tissue layers that commonly occurs 3 to 11 days after injury.
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Evisceration
Protrusion of visceral organs through a wound opening.
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Fistula
Abnormal passage between two organs or between and organ and the surface of
the body